We have recently described a new complement (C) function, the solubilization of immune complexes. The present proposal deals with the mechanism of this reaction and characterization of its end-product, that is, the "released" complexes, which contain antigen, antibody, C3 and probably other C components. In view of the profound effects of C on the degree of aggregation, size, and molecular composition of complexes, "released" complexes probably have different biological and pathological activity from "non-released" complexes. Indeed, we found that released complexes do not bind to the membrane of platelets and leukocytes. Because antigen-antibody complexes (without C) induce the release of potent mediators of inflammation from cells, it is conceivable that the C system plays a hitherto unsuspected role of protecting the body from potentially damaging complexes. For this reason, we will re-examine the consequences of in vivo decomplementation of animals in the immunopathology of experimental glomerulonephritis. A separate objective of this proposal is to clarify the relation between IgD/IgM-bearing cells and complement receptor (CR) lymphocytes. This information may validate the use of the CR as a membrane marker of circulating B lymphocytes.